Endocrine Abstracts

The rapidly increasing incidence of T1D worldwide and studies among migrants have shown that environmental factors play an important role in the pathogenesis of T1D. Identification of these risk-modulating factors would offer an excellent opportunity to develop effective strategies for prevention of T1D. Vitamin D is one of the main candidates for protection from type 1 diabetes, although prospective epidemiological studies on the effect of vitamin D exposure during pregnancy, infancy and childhood have given inconsistent results. Vitamin D regulates the immune system and autoimmunity, which could be of relevance in the pathogenesis of type 1 diabetes. According to a prospective Norwegian study, high vitamin D status (25-OH vitamin D concentration) during the last trimester was inversely associated with the risk of type 1 diabetes in the offspring, whereas in a comparable Finnish study, vitamin D status during the first trimester was not associated with the disease risk. Recently, maternal vitamin D receptor (VDR) variants were found to be associated with a child’s risk of type 1 diabetes independently of the child’s genotype suggesting early programming of type 1 diabetes in the fetus. In north Finland 1965 birth cohort, vitamin D supplementation during infancy were inversely associated with type 1 diabetes development, whereas occurrence of rickets was directly associated with the disease. It is noteworthy that vitamin D supplementation recommendations were high at that time in Finland (50 μg/day). Recently findings from international TEDDY Study showed that childhood vitamin D status was protectively associated with islet autoimmunity and that association was modified by one SNIP of VDR. Interactions between genes and vitamin D intake/status on the development of islet autoimmunity and type 1 diabetes may explain the inconsistent findings. Vitamin D metabolism genes are associated with development of islet autoimmunity and type 1 diabetes as well as with vitamin D status.